Platelet-activating factor (PAF) is a phospholipid mediator that exhibits diverse and potent effects on many cell types (1). PAF is a potent mediator of hypersensitivity and inflammatory reactions (2). Type 1 diabetes is caused by autoimmune destruction of the β-cells in the pancreas, which is initiated years before the clinical presentation of disease (3). In recent-onset type 1 diabetes and in animal models of autoimmune diabetes, a characteristic pathological finding in the islets of Langerhans is the accumulation of mononuclear cells and β-cell death (insulitis) (4,5). In this study, we investigated the role of PAF as an inflammatory mediator in pathogenesis of type 1 diabetes, which is a chronic inflammatory process.
Serum PAF levels of 38 type 1 diabetic patients and 22 healthy children with an age range of 5–15 years were evaluated by a high-performance liquid chromatography method. Statistical analysis was performed by the nonparametric Kruskall-Wallis and Mann-Whitney U tests. Average serum PAF levels of patients and healthy children were measured to be 445.11 ± 55.79 and 198.0 ± 80.0 pg/ml, respectively. Serum PAF levels of the patient group were significantly higher than those of the healthy children (P < 0.01). The patients were divided into three groups according to the duration of diabetes as newly diagnosed, 3 months to 5 years, and >5 years. Average serum PAF levels in these groups were 757.8 ± 82.2, 307.3 ± 27.1, and 387.0 ± 57.9 pg/ml, respectively. In the newly diagnosed patient group, serum PAF levels were found to be significantly higher than those of the other groups (P < 0.01). There was no significant difference in serum PAF levels between the group with diabetes duration of 3 months to 5 years and that with diabetes duration >5 years (P > 0.01).
Serum PAF levels of patients with type 1 diabetes were significantly higher than the healthy group. When patients were divided into the three groups according to duration of diabetes, the highest levels were observed in patients with newly diagnosed diabetes. These results may indicate that PAF plays a role in the development of type 1 diabetes. There are few reports on this issue. In an experimental study about the role of PAF in the development of type 1 diabetes, it was detected that administration of recombinant PAF-acetyl hydrolase, which inactivates PAF to rats, caused a decrease in insulitis (6). Another experimental study reported that the PAF synthesis capacity of polymorphonuclear leukocytes was increased in diabetic rats (7).
There is also clinical research that reports an increased serum level of PAF in type 1 diabetes. However, in these studies, increased levels of PAF were attributed to the ongoing hyperglycemia and were thought to accentuate the development of micro- and macrovascular complications (8,9). In our study, high levels of PAF detected in patients who had diabetes for a long duration when compared with the healthy group might be associated with vascular complications.
In conclusion, PAF levels are increased in children with type 1 diabetes. This increment was higher in children with new-onset diabetes and may be important in the etiopathogenesis of type 1 diabetes. Further research supporting the use of PAF antagonists in patients with new-onset diabetes is required.
